Date published: 2026-10-8

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FRRS1 CRISPR/Cas9 KO Plasmid (m): sc-422860

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • FRRS1 CRISPR/Cas9 Knockout (KO) Plasmid (m) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
  • gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the FRRS1 genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
  • The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    FRRS1 CRISPR/Cas9 KO Plasmid (m)

    sc-422860
    20 µg
    $397.00

    Overview

    Frrs1 encodes FRRS1, an endoplasmic reticulum–associated protein implicated in the maturation and functional regulation of AMPA-type glutamate receptors. In neurons, FRRS1 participates in glutamatergic synapse development and excitatory neurotransmission by supporting receptor assembly/trafficking and synaptic receptor availability. Disruption of FRRS1-linked processes can alter synaptic signaling homeostasis and neuronal network activity, making Frrs1 a relevant target for studying mechanisms underlying neurodevelopmental and neurological phenotypes. Mouse Frrs1 models are therefore useful for dissecting receptor biogenesis pathways and synaptic plasticity-related cellular programs.

    FRRS1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Frrs1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Frrs1 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.

    The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the Frrs1 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish FRRS1 protein expression.

    This CRISPR knockout system enables efficient generation of Frrs1-deficient cell models for investigation of FRRS1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Frrs1 exon(s) critical for FRRS1 function
    • Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
    • GFP reporter for identification of transfected cells
    • Pool of plasmids targeting multiple Frrs1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by FRRS1 CRISPR/Cas9 KO Plasmid (m) and FRRS1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Frrs1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by FRRS1 HDR Plasmid (m) and FRRS1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Frrs1 homology arms to support homology-directed repair at defined Frrs1 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.

    For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.